Evidence map›Paper›PMID 29698390›Full record

ArticleActa pharmacologica Sinica2018

MicroRNA expression profile and functional analysis reveal their roles in contact inhibition and its disruption switch of rat vascular smooth muscle cells.

Ye-Ying Sun, Shan-Shan Qin, Yun-Hui Cheng, Chao-Yun Wang, Xiao-Jun Liu, Ying Liu, Xiu-Li Zhang, Wendy Zhang, Jia-Xin Zhan, Shuai Shao and 6 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmacologica Sinica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 37% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 2 countries.

Ye-Ying SunSino-US Translational Medicine Institute and College of Pharmacy, Binzhou Medical University, Yantai 264003, China.
Shan-Shan QinDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Yun-Hui ChengDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Chao-Yun WangSino-US Translational Medicine Institute and College of Pharmacy, Binzhou Medical University, Yantai 264003, China.
Xiao-Jun LiuDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Ying LiuDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Xiu-Li ZhangSino-US Translational Medicine Institute and College of Pharmacy, Binzhou Medical University, Yantai 264003, China.
Wendy ZhangDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Jia-Xin ZhanDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Shuai ShaoDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Wei-Hua BianSino-US Translational Medicine Institute and College of Pharmacy, Binzhou Medical University, Yantai 264003, China.
Bi-Hui LuoDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Dong-Feng LuDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Jian YangDepartment of Biomedical Engineering, School of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Chun-Hua WangSino-US Translational Medicine Institute and College of Pharmacy, Binzhou Medical University, Yantai 264003, China.
Chun-Xiang ZhangSino-US Translational Medicine Institute and College of Pharmacy, Binzhou Medical University, Yantai 264003, China.
University of Alabama at Birmingham · USBinzhou Medical University · CNBinzhou University · CN

Funding

GOLPH3 in vascular smooth muscle cell biology and vascular diseaseR01HL130052 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI QIN, GANGJIAN · 2016 to 2019
$1.5M
NHLBI NIH HHS R01 HL130052
6 · The paper itself

Abstract

Contact inhibition and its disruption of vascular smooth muscle cells (VSMCs) are important cellular events in vascular diseases. But the underlying molecular mechanisms are unclear. In this study we investigated the roles of microRNAs (miRNAs) in the contact inhibition and its disruption of VSMCs and the molecular mechanisms involved. Rat VSMCs were seeded at 30% or 90% confluence. MiRNA expression profiles in contact-inhibited confluent VSMCs (90% confluence) and non-contact-inhibited low-density VSMCs (30% confluence) were determined. We found that multiple miRNAs were differentially expressed between the two groups. Among them, miR-145 was significantly increased in contact-inhibited VSMCs. Serum could disrupt the contact inhibition as shown by the elicited proliferation of confluent VSMCs. The contact inhibition disruption accompanied with a down-regulation of miR-145. Serum-induced contact inhibition disruption of VSMCs was blocked by overexpression of miR-145. Moreover, downregulation of miR-145 was sufficient to disrupt the contact inhibition of VSMCs. The downregulation of miR-145 in serum-induced contact inhibition disruption was related to the activation PI3-kinase/Akt pathway, which was blocked by the PI3-kinase inhibitor LY294002. KLF5, a target gene of miR-145, was identified to be involved in miR-145-mediated effect on VSMC contact inhibition disruption, as it could be inhibited by knockdown of KLF5. In summary, our results show that multiple miRNAs are differentially expressed in contact-inhibited VSMCs and in non-contact-inhibited VSMCs. Among them, miR-145 is a critical gene in contact inhibition and its disruption of VSMCs. PI3-kinase/Akt/miR-145/KLF5 is a critical signaling pathway in serum-induced contact inhibition disruption. Targeting of miRNAs related to the contact inhibition of VSMCs may represent a novel therapeutic approach for vascular diseases.

Indexed as

AnimalsCell CountCell ProliferationChromonesContact InhibitionDown-RegulationKruppel-Like Transcription FactorsMaleMicroRNAsMorpholinesMuscle, Smooth, VascularMyocytes, Smooth MusclePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktRats, Sprague-Dawley2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesKlf5 protein, ratKruppel-Like Transcription FactorsMicroRNAsMIRN145 microRNA, ratMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID29698390
PMCPMC5943918
OpenAlexW2802994650

What OpenQuestion holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.